Partial Pressure of Arterial Oxygen

Depending on the efficacy of gas exchange, the alveolar oxygen partial pressure (tension) tends to equilibrate with the mixed venous blood, resulting in the Pao₂, which determines the degree of oxygen saturation of hemoglobin. In addition to its chemical combination with hemoglobin, oxygen is also dissolved in plasma and red blood cells (RBCs). Most of the oxygen in whole blood is bound to hemoglobin (measured clinically as oxygen saturation), whereas the amount of dissolved oxygen is only a small fraction of the total quantity carried in whole blood.

The quantity of oxygen bound to hemoglobin depends on the Pao₂ and the oxygen dissociation curve (Figure 71-3). The blood is almost completely saturated at a Pao₂ of 90 to 100 mm Hg. The flattening of the upper portion of the S-shaped dissociation curve makes it virtually impossible to estimate oxygen tension greater than 60 to 80 mm Hg by using arterial oxygen saturation alone. The dissociation curve of fetal hemoglobin (compared with adult hemoglobin) is shifted to the left, and at any Pao₂ less than 100 mm Hg, fetal blood binds more oxygen. The shift appears to be the result of the lower affinity of fetal hemoglobin for 2,3-diphosphoglycerate. Note that pH, Paco₂, temperature, and diphosphoglycerate (DPG) content influence the position of the dissociation curve.

Arterial oxygen content (Cao₂) is the sum of hemoglobin-bound and dissolved oxygen, as described by the following equation:

where the arterial oxygen content is in mL/100 mL of blood, 1.37 is the approximate amount of oxygen (in milliliters) bound to 1 g of hemoglobin at 100% saturation, Hb is hemoglobin concentration (g/100 mL), Sao₂ is the percentage of hemoglobin bound to oxygen, and 0.003 is the solubility factor of oxygen in plasma (mL/mm Hg). In this equation, the first term (1.37 × Hb × Sao₂) is the amount of oxygen bound to hemoglobin. The second term (0.003 × Pao₂) is the amount of oxygen dissolved in plasma and red blood cells.

Most of the oxygen in the blood is carried by hemoglobin. For example, if an infant has a Pao₂ of 80 mm Hg, an Sao₂ of 99%, and a hemoglobin concentration of 15 g/100 mL, Cao₂ is the sum of oxygen bound to hemoglobin ([1.37 × 15 × 99]/100 = 20.3 mL) plus the oxygen dissolved in plasma (0.003 × 80 = 0.24 mL). In this example, just over 1% of oxygen in blood is dissolved in plasma and almost 99% is carried by hemoglobin.

The partial pressure of oxygen in arterial blood not only depends on the ability of the lungs to transfer oxygen as determined by alveolar ventilation, but also is largely influenced by the . For normal gas exchange, the ventilation and perfusion should be proportional. The ratio should be very close to 1 : 1; that is, for every milliliter of gas that passes the alveoli, there should be a proportional volume of blood in the pulmonary capillary bed. If the is decreased (as in RDS), only partial oxygenation and CO₂ removal from the mixed venous blood will occur. Oxygen supplementation can largely overcome the hypoxemia when the is decreased. If the is high, as in overventilation, partial pressure of oxygen is increased slightly.

The mechanism of shunting becomes evident when blood bypasses the alveoli, as occurs in congenital cyanotic heart disease, persistent pulmonary hypertension, or atelectasis. Oxygen supplementation does not prevent the hypoxemia produced by such a shunt. Hypoventilation (e.g., caused by apnea) is a common cause of hypoxemia. Diffusion limitation can affect oxygenation slightly, but this mechanism is not a common cause of severe hypoxemia in neonates. Hypoxemia caused by either hypoventilation or diffusion limitation usually can be treated easily with oxygen supplementation.

Three indexes can be used to estimate the degree of oxygenation derangement (see Chapter 78). The arterial-alveolar oxygen tension ratio (Pao₂/Pao₂ or a/ao₂ ratio) has no units, decreases with worsening oxygenation, and can be obtained from the equation

where R is the respiratory quotient. Because [Fio₂ + (1 − Fio₂)/R] approximates 1.0 and Paco₂ approximates Paco₂, the equation can be simplified as follows:

The alveolar-arterial oxygen tension gradient (Pao₂ − Pao₂ or AaDO₂) is expressed in mm Hg, increases with worsening oxygenation, and can be obtained from the equation

or

The oxygenation ratio is expressed in mm Hg, decreases with worsening oxygenation, and can be obtained from the equation

The oxygenation ratio is less often used because it is subject to inaccurate assessment of the oxygenation derangement when Paco₂ varies markedly. Often it is necessary to correct the degree of oxygenation for the ventilatory support because oxygenation is strongly influenced by mean airway pressure () during assisted ventilation. The oxygenation index (OI) is useful under these circumstances. The OI, which increases with worsening oxygenation or increasing , has units of centimeters of water per mm Hg and can be obtained by the equation

Partial Pressure of Arterial Carbon Dioxide

Paco₂ is an important measure of pulmonary function in neonatal respiratory disease. Mechanisms responsible for impairment of pulmonary exchange of CO₂ include hypoventilation, mismatch, and shunt. In addition, an increase in dead space, as occurs with alveolar overdistention or gas trapping, impairs CO₂ elimination. Because of the high solubility coefficient of CO₂, diffusion limitation rarely affects CO₂ exchange. As tissue levels of CO₂ increase above those of arterial blood, molecules diffuse into the capillaries and are transported in RBCs and plasma. Unlike the S-shaped dissociation curve for O₂, the relationship between CO₂ tension and content is almost linear over the physiologic range.

Carbon Dioxide

Noninvasive estimates of CO₂ by end-tidal or transcutaneous detectors provide a reasonable alternative to frequent blood gas sampling, allowing for continuous monitoring of CO₂ over prolonged periods of time. End-tidal CO₂ monitoring is a noninvasive technique that measures CO₂ concentration in the gas at the end of expiration. Quantitative measurements of end-tidal CO₂ have been shown to correlate well with arterial blood gases in term and preterm infants without pulmonary disease and can be useful for detection of rapid changes in exhaled CO₂ with data displayed on a breath-by-breath basis.⁵³ When there is minimal pulmonary disease, quantitative end-tidal CO₂ monitoring can assist in detection of hypercapnia and hypocapnia. However, with small tidal volumes and high respiratory rates it may underestimate the true alveolar gas in some neonates. Alternative designs, such as disposable colorimetric end-tidal CO₂ detectors, have a high diagnostic accuracy for confirmation of endotracheal tube placement.⁷⁷ A positive end-tidal CO₂ test confirms endotracheal tube placement, and a negative test strongly suggests esophageal intubation. However, many infants can have falsely negative results at birth.⁶²

Transcutaneous CO₂ detectors have been shown to be superior to end-tidal CO₂ in ill neonates.⁵³ However, sensor preparation, taping, and the need for changes in sensor location may limit transcutaneous CO₂ usefulness. Despite the limitations of end-tidal and transcutaneous monitoring of CO_2, these methods provide critically important continuous information pertaining to changes in the respiratory system and minimize the need for blood gas analysis.

Oxygen

Maintenance of oxygenation in an acceptable range requires constant monitoring that is not possible with intermittent blood gas measurements. This has led to the widespread implementation of pulse oximetry as a means of continuous noninvasive O₂ monitoring (see Chapter 71). Pulse oximetry measures the amount of hemoglobin molecules that is bound with oxygen. It has a rapid response time and can be used as an estimate of Pao₂ for detecting short intermittent hypoxic episodes. However, as shown by the oxyhemoglobin dissociation curve (see Figure 71-3), oxygen saturation levels should remain below 95% in infants requiring supplemental O₂ as hyperoxic values of Pao₂ cannot be distinguished beyond that range.